In the heart, natural atrial electrical depolarization waves propagate from the sinus node through the atrium to the atrioventricular node to stimulate the ventricle. In some diseased hearts, the electrical conduction pathway breaks down, so that the sinus node triggers the electrical heartbeat process but the electrical impulse does not conduct to the ventricle.
Dual-chamber pacemakers adapt pacing rate and timing to a patient's needs by sensing natural atrial heartbeat signals (P-waves) and by generating electrical stimulating pulses in the ventricle in response to the timing of sensed P-waves. The ideal sensor for determining a proper pacing rate is a normally functioning sinus node. Physiologic pacemakers which employ atrial sensing in VDD and DDD pacing modes, as are standard in the art of pacemakers, are truly rate responsive. Dual-chamber pacing is an effective therapy for high degree atrioventricular block, particularly for patients in which the natural sinus (rate-determining) mechanism is intact and functioning normally. In such cases, the rate-determining response of the pacemaker to emotion or exertion is the same as that of the normal heart's rate-setting mechanisms. Thus, the pacemaker acts as an artificial atrioventricular conducting system to reestablish A-V synchrony.
One disadvantage of a standard dual-chamber pacemaker is that it requires implantation of an atrial lead. An atrial lead presents multiple technical problems which arise from the anatomical and physiological nature of the atrium. The atrial wall is much thinner than the ventricular wall. Implanting a lead in the atrium is more likely to injure cardiac tissue, leading to difficulties in sensing natural atrial signals and possibly causing tissue scarring, resulting in dangerous arrhythmia conditions.
A ventricular lead can hold its electrode position with more stability than can an atrial lead. Leads are difficult to "fix" within atrial tissue in a stable position which is conducive to effective cardiac signal sensing. An atrial electrode which is not firmly affixed may cause intermittent P-wave sensing.
Pacing the atrial chamber is difficult due to the difficulty in affixing the atrial electrode to the thin atrial tissue. Furthermore, atrial stimulation may induce atrial arrhythmias such as atrial fibrillation.
Furthermore, the requirement for two leads in standard dual-chamber pacemakers leads to an increase in logical complexity, intensifying the dangers of improper interactions between control operations involved in pacing the two chambers, due to errors in programming variables which control the pacing interaction and the occurrence of unforeseen physiological events which disrupt the control pattern between the two heart chambers. With two leads, twice the danger of injury to heart tissue exists. Furthermore, a dual lead system is inherently more expensive than a single lead pacemaker.
Excessive current drain is an additional disadvantage of dual-lead pacemakers. In addition, a single lead pacemaker is much preferable for patients having a small vein diameter, such as children.
One manner of addressing the disadvantages of standard dual-chamber pacing was to perform single-chamber pacing in the ventricle (VVI) while including an extra sensor in the ventricle which did not generate atrial stimulation pulses, but merely sensed atrial cardiac activity. Knudson et al. in U.S. Pat. No. 4,313,442, entitled "Atrial Rate Sensitive Cardiac Pacer Apparatus", issued Feb. 2, 1982, described a pacemaker with a single lead implanted in the ventricle of the heart which sensed cardiac atrial signals to determine cardiac demand and altered cardiac output to satisfy that demand. The lead had an electrode at its distal end implanted in the ventricle of the heart for sensing ventricular cardiac electrical signals and for stimulating ventricular pacing pulses. In addition, the lead had a second electrode located proximal to the first in a manner such that it was situated within the atrium of the heart. The second electrode sensed cardiac electrical signals arising from the atrium. Changes in atrial electrical cycle intervals were detected and averaged over multiple cardiac cycles to provide a control signal which was used to modulate the ventricular heart rate and, consequently, cardiac output. Wright et al. in U.S. Pat. No. 4,298,007, entitled "Atrial Rate Sensitive Cardiac Pacer Circuit", issued Nov. 3, 1981, described a circuit which performed the operations designated in the Knudson et al. patent. In this pacemaker, the lead was capable of sensing atrial depolarization, but atrial pacing was not possible since the electrode was not in contact with the atrial wall.
A number of problems arose in the Knudson et al. and Wright et al. systems. First, implantation of the ventricular electrode involved critical logistic problems. The ventricular electrode required implantation such that the atrial electrode was positioned where it could properly sense atrial depolarizations. A physician needed to implant the ventricular electrode, then test the atrial electrode for positioning and atrial signal sensing. If the position was not correct, the physician was required to remove the lead and attempt a second lead implantation using a lead with a different distance between the atrial and ventricular electrodes. Changing the leads was extremely difficult. Using subclavian punctures, a large introducing cannula (in situ) was required to confirm the occurrence of adequate atrial sensing. This implantation procedure was extremely difficult, cumbersome, prolonged and expensive. Furthermore, after the operation, atrial sensing was not always reliable and P-wave amplitudes were often inadequate.
A second problem with the Knudson et al. and Wright e al. pacemakers was that, in contrast to single chamber ventricular pacemakers, they required a special lead with separate electrodes for the atrium and the ventricle. A major disadvantage of the lead was its large size which was necessary to enclose three conductors. This lead was not standard for cardiac pacing and required additional electronics within the pacemaker which may increase the size and energy requirements of the electronics within the pacemaker, leading to an increased pacemaker size or a decreased service lifetime. Furthermore, it was often desirable to implant a new pacemaker and attach it to previously implanted leads. The Knudson et al. and Wright et al. pacemakers could not be attached to leads other than the required special leads.
A third problem with the Knudson et al. and Wright et al. pacemakers was that the atrial lead was free-floating in the atrial chamber of the heart, leading to inconsistent sensing of atrial signals.
A fourth problem existed in the Knudson et al. and Wright et al. pacemakers. Because sensing was not reliable, the pacemakers did not provide for P-waves to trigger ventricular pacing, but instead P-wave intervals were detected and averaged to determine the ventricular pacing rate. The pacemakers did not perform synchronous pacing so, unlike the result of a pacemaker operating in VDD or DDD pacing mode, there was no boost to cardiac hemodynamic output. The pacemakers were not as efficient as conventional DDD pacemakers.
J.C.P. Crick in "European Multicenter Prospective Follow-Up Study of 1,002 Implants of a Single Lead VDD Pacing System", PACE. Vol. 14, pages 1742-1744 (1991), discusses a pacemaker which solves the fourth stated problem afflicting the Knudson et al. and Wright et al. system by providing for sensing of P-waves and triggering of ventricular pacing pulse generation. However, the pacemaker discussed by Crick does require a special pacing lead which includes an electrode which is implanted within the atrium, the second stated disadvantage of the Knudson et al. and Wright et al. pacemakers.
When a heart's natural sinus mechanism is not operating properly, a ventricular rate responsive pacemaker may better provide for physiological rate-determination than a DDD pacemaker. However, an important limitation of rate responsive ventricular pacing arises upon the occurrence of retrograde conduction, wherein a depolarizing impulse from the ventricular myocardium is transmitted to the atrial myocardium, possibly triggering dangerous ventricular arrhythmias or generating cannon A-waves. Cannon A-waves are large abrupt waves in the jugular venous pulse that occur when the respectively contract against a closed tricuspid valve and a closed bicuspid valve due to atrioventricular asynchrony or ventricular tachycardia. For patients suffering from retrograde conduction, the addition of a sensor to increase pacing rate with exercise will not improve the cardiac output but rather will depress it even further. Therefore, the implantation of a ventricular rate responsive pacemaker may be contraindicated in some of the patients for whom it has been specifically designed, patients with the sick sinus syndrome and chronotropic dysfunction but who have intact ventriculo-atrial conduction.